With age a large percentage of the population develops atherosclerotic arterial obstructions causing a diminished blood circulation and blood clots 7hich further diminish or block the blood flow. When this process occurs in a coronary artery it is referred to as a heart attack. Commonly such conditions are treated surgically by grafting a bypass, or by less invasive procedures such as angioplasty or atherectomy. These less invasive procedures are less traumatic to the patient, are usually performed under local anesthesia, a brief hospitalization is usually sufficient and their direct and indirect costs are a fraction as compared to by-pass surgery. A major shortcoming of angioplasty is a high rate of re-closure of the artery or "restenosis". Angioplasty does not remove the obstruction but instead it radially displaces the atherosclerotic plaque and often tears the arterial wall. This triggers excessive proliferation of smooth muscle cell in the medial arterial layer (hyperplasia) and blood clotting, which are the major causes of restenosis of the newly created lumen (neolumen). Additionally elastic recoil of the arterial wall partially negates the effect of angioplasty.
An objective of the present invention minimizes restenosis by: A) Extracting the plaque, thereby minimize the elastic recoil B) Forming a smooth continuous lumen, thereby minimizing blood clotting C) Minimizing injury to the arterial wall, thereby minimizing hyperplasia D) Applying restenosis inhibiting drugs to the atherectomy site which inhibit blood clotting and hyperplasia proliferation. Drugs which are currently accepted, or being evaluated, for such purpose are, for example: 1) Hirudin, which blocks thrombin-platelet receptors preventing platelet aggregation and subsequent release of platelet derived growth factor (PDGF) which stimulates hyperplasia 2) Low-molecular weight heparin, the non-anticoagulant fragment of heparin believed to directly alter the smooth muscle cells' life cycle 3) Glucocorticoids, which are steroids believed to inhibit the production of PDGF-like material by smooth muscle cells and the radial migration of smooth muscle cells through the arterial wall 4) Angiopeptin, a peptitde analogue of Somatostatin believed to inhibit smooth muscle cell production of a hyperplasia causing growth factor 5) Angiotensin converting enzyme inhibitor, which is believed to inhibit hyperplasia 6) Anti-mitogenics, which directly inhibit hyperplasia 7) Antiplatelets antibodies, which reduce the release of PDGF 8) Endotilin neutralizer which inhibits the vasoconstriction and cell proliferation caused by Endotilin which is secreted by injured endothal cells. It can be appreciated that there is on-going research in this area which periodically suggests that additional drugs would fit this category of restenosis inhibiting drugs, and such drugs may also be applied to the atherectomy site by this system. Additional information on such research may be found in the abstracts published by the Division of Cardiology, Department of Internal Medicine, of the University of Michigan in Ann Arbor covering a conference held in May 17-18, 1990 Titled the Restenosis Summit II.
Another objective is to provide a system that can be made in large and small diameters, down to approximately 1 mm (millimeter) and a length of approximately a meter, to reach and enter small and remote arteries. A further objective is to utilize the physician's existing skills accessing the artery and placing a guide wire through the obstruction.
The above and other objectives of the invention will become apparent from the following discussion and the accompanying drawings.